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ABC OF INTERVENTIONAL CARDIOLOGY – PART 5 pot

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Note the difference between left ventricular peak pressure and aortic peak pressure, which represents the left ventricular outflow tract gradient, has been reduced from 80 mm Hg to 9 mm

Trang 1

Heart block is a frequent acute complication, so a temporary

pacing electrode is inserted via the femoral vein beforehand

and is usually left in situ for 24 hours after the procedure,

during which time the patient is monitored

The main procedural complications are persistent heart

block requiring a permanent pacemaker (10%), coronary artery

dissection and infarction requiring immediate coronary artery

bypass grafting (2%), and death (1-2%) The procedural

mortality and morbidity is similar to that for surgical myectomy,

as is the reduction in left ventricular outflow tract gradient

Surgery and ethanol septal ablation have not as yet been

directly compared in randomised studies

Septal defect closure

Atrial septal defects

Atrial septal defects are congenital abnormalities characterised

by a structural deficiency of the atrial septum and account for

about 10% of all congenital cardiac disease The commonest

atrial septal defects affect the ostium secundum (in the fossa

ovalis), and most are suitable for transcatheter closure Although

atrial septal defects may be closed in childhood, they are the

commonest form of congenital heart disease to become

apparent in adulthood

Diagnosis is usually confirmed by echocardiography,

allowing visualisation of the anatomy of the defect and Doppler

estimation of the shunt size The physiological importance of

the defect depends on the duration and size of the shunt, as well

as the response of the pulmonary vascular bed Patients with

significant shunts (defined as a ratio of pulmonary blood flow to

systemic blood flow > 1.5) should be considered for closure

when the diagnosis is made in later life because the defect

reduces survival in adults who develop progressive pulmonary

hypertension They may also develop atrial tachyarrhythmias,

which commonly precipitate heart failure

Patients within certain parameters can be selected for

transcatheter closure with a septal occluder In those who are

unsuitable for the procedure, surgical closure may be considered

Patent foramen ovale

A patent foramen ovale is a persistent flap-like opening

between the atrial septum primum and secundum which occurs

in roughly 25% of adults With microbubbles injected into a

peripheral vein during echocardiography, a patent foramen

ovale can be demonstrated by the patient performing and

Simultaneous aortic and left ventricular pressure waves before (left) and after (right) successful ethanol septal ablation Note the difference

between left ventricular peak pressure and aortic peak pressure, which represents the left ventricular outflow tract gradient, has been

reduced from 80 mm Hg to 9 mm Hg

Indications and contraindications for percutaneous closure

of atrial septal defects Indications

Clinical

x If defect causes symptoms

x Associated cerebrovascular embolic event

x Divers with neurological decompression sickness

Anatomical

x Defects within fossa ovalis (or patent foramen ovale)

x Defects with stretched diameter < 38 mm

Contraindications

x Sinus venosus defects

x Ostium primum defects

x Pulmonary:systemic flow ratio

> 1.5 and reversible pulmonary hypertension

x Right-to-left atrial shunt and hypoxaemia

x Presence of > 4 mm rim of tissue surrounding defect

x Ostium secundum defects with other important congenital heart defects requiring surgical correction

Deployment sequence of the Amplatzer septal occluder for closing an atrial septal defect

Micrograph of hypertrophied myocytes in haphazard alignments characteristic of hypertrophic

cardiomyopathy Interstitial collagen is also increased

Trang 2

releasing a prolonged Valsalva manoeuvre Visualisation of

microbubbles crossing into the left atrium reveals a right-to-left

shunt mediated by transient reversal of the interatrial pressure

gradient

Although a patent foramen ovale (or an atrial septal

aneurysm) has no clinical importance in otherwise healthy

adults, it may cause paradoxical embolism in patients with

cryptogenic transient ischaemic attack or stroke (up to half of

whom have a patent foramen ovale), decompression illness in

divers, and right-to-left shunting in patients with right

ventricular infarction or severe pulmonary hypertension

Patients with patent foramen ovale and paradoxical embolism

have an approximate 3.5% yearly risk of recurrent

cerebrovascular events

Secondary preventive strategies are drug treatment (aspirin,

clopidogrel, or warfarin), surgery, or percutaneous closure using

a dedicated occluding device A lack of randomised clinical

trials directly comparing these options means optimal

treatment remains uncertain However, percutaneous closure

offers a less invasive alternative to traditional surgery and allows

patients to avoid potential side effects associated with

anticoagulants and interactions with other drugs In addition,

divers taking anticoagulants may experience haemorrhage in

the ear, sinus, or lung from barotrauma

Congenital ventricular septal defects

Untreated congenital ventricular septal defects that require

intervention are rare in adults Recently, there has been interest

in percutaneous device closure of ventricular septal defects

acquired as a complication of acute myocardial infarction

However, more experience is necessary to assess the role of this

procedure as a primary closure technique or as a bridge to

subsequent surgery

The picture of a stenotic mitral valve and micrograph of myocytes showing

hypertrophic cardiomyopathy were provided by C Littman, consultant

histopathologist at the Health Sciences Centre, Winnipeg, Manitoba,

Canada The postmortem picture of a heart with hypertrophic

cardiomyopathy was provided by T Balachandra, chief medical examiner for

the Province of Manitoba, Winnipeg The pictures of Amplatzer occluder

devices were provided by AGA Medical Corporation, Minnesota, USA.

Amplatzer occluder devices for patent foramen ovale (left) and muscular ventricular septal defects (right)

Further reading

x Inoue K, Lau K-W, Hung J-S Percutaneous transvenous mitral

commissurotomy In: Grech ED, Ramsdale DR, eds Practical

interventional cardiology 2nd ed London: Martin Dunitz, 2002:

373{87

x Bonow RO, Carabello B, de Leon AC, Edmunds LH Jr, Fedderly

BJ, Freed MD, et al ACC/AHA guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with

Valvular Heart Disease) J Am Coll Cardiol 1998;32:1486-582

x Wilkins GT, Weyman AE, Abascal VM, Bloch PC, Palacios IF Percutaneous balloon dilatation of the mitral valve: an analysis of echocardiographic variables related to outcome and the

mechanism of dilatation Br Heart J 1998;60:299-308

x Wigle ED, Rakowski H, Kimball BP, Williams WG Hypertrophic

cardiomyopathy: clinical spectrum and treatment Circulation 1995;

92:1680-92

x Nagueh SF, Ommen SR, Lakkis NM, Killip D, Zoghbi WA, Schaff

HV, et al Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive

cardiomyopathy J Am Coll Cardiol 2001;38:1701-6

x Braun MU, Fassbender D, Schoen SP, Haass M, Schraeder R, Scholtz W, et al Transcatheter closure of patent foramen ovale in

patients with cerebral ischaemia J Am Coll Cardiol 2002;39:

2019-25

x Waight DJ, Cao Q-L, Hijazi ZM Interventional cardiac catheterisation in adults with congenital heart disease In: Grech

ED, Ramsdale DR, eds Practical interventional cardiology 2nd ed.

London: Martin Dunitz, 2002:390-406

ABC of Interventional Cardiology

Trang 3

Julian Gunn, Ever D Grech, David Crossman, David Cumberland

Percutaneous coronary intervention has become a more

common procedure than coronary artery bypass surgery in

many countries, and the number of procedures continues to

rise In one day an interventionist may treat four to six patients

with complex, multivessel disease or acute coronary syndromes

Various balloons, stents, and other devices are delivered by

means of a 2 mm diameter catheter introduced via a peripheral

artery The success rate is over 95%, and the risk of serious

complications is low After a few hours patients can be

mobilised, and they are usually discharged the same or the next

day Even the spectre of restenosis is now fading

Refinements of existing techniques

The present success of percutaneous procedures is largely

because of refinement of our “basic tools” (intracoronary

guidewires and low profile balloons), which have greatly

contributed to the safety and effectiveness of procedures

However, the greatest technological advance has been in the

development of stents These are usually cut by laser from

stainless steel tubes into a variety of designs, each with different

radial strength and flexibility They are chemically etched or

electropolished to a fine finish and sometimes coated

Digital angiography is a great advance over cine-based

systems, and relatively benign contrast media have replaced the

toxic media used in early angioplasty Although magnetic

resonance and computed tomographic imaging may become

useful in the non-invasive diagnosis of coronary artery disease,

angiography will remain indispensable to guide percutaneous

interventions for the foreseeable future

New device technology

Pre-eminent among new devices is the drug eluting (coated)

stent, which acts as a drug delivery device to reduce restenosis

The first of these was the sirolimus coated Cypher stent

Triple vessel disease is no longer a surgical preserve, and particularly good results are expected with drug eluting stents In this case, lesions in the left anterior descending (LAD), circumflex (Cx), and right coronary arteries (RCA) (top row) are treated easily and rapidly by stent (S) implantation (bottom row)

Performance of percutaneous coronary intervention General statistics

x Success rate of procedure > 95%

x Symptoms improved after procedure 90%

x Restenosis 15% (range 5-50%)

x Duration of procedure 15 minutes-3 hours

x Access point:

Radial or brachial artery 5%

x Time in hospital after procedure:

x Intravenous contrast load 100-800 ml

x X ray dose to patient 75 Gy/cm 2

Special conditions

x Success of direct procedure for acute myocardial infarction > 95%

x Success for chronic ( > 3 month) occluded vessel 50-75%

x Mortality for procedure in severe cardiogenic shock 50%

x Restenosis:

Vessels < 2.5 mm in diameter, > 40 mm length 60% Vessels > 3.5 mm diameter, < 10 mm length 5%

x Lesion recurrence later than 6 months after procedure < 5%

x Re-restenosis:

After repeat balloon dilatation 30-50% After brachytherapy < 15%

*Death, myocardial infarction, coronary artery bypass surgery, cerebrovascular accident

†Equivalent to 1-2 computed tomography scans

Interventional devices and their uses

Stent 70-90% Most types

Drug eluting stent 0-50% High risk of restenosis

(possibly all) Cutting balloon 1-5% In-stent restenosis, ostial

lesions Rotablator 1-3% Calcified, ostial, undilatable

lesions Brachytherapy 1-3% In-stent restenosis

Atherectomy < 1% Bulky, eccentric, ostial lesions

Stent graft < 1% Aneurysm, arteriovenous

malformation, perforation Thrombectomy < 1% Visible thrombus

Laser < 1% Occlusions, in-stent restenosis

Distal protection < 1% Degenerate vein graft

Trang 4

Sirolimus is one of several agents that have powerful antimitotic

effects and inhibit new tissue growth inside the artery and stent

In a randomised controlled trial (RAVEL) this stent gave a six

month restenosis rate of 0% compared with 27% for an

uncoated stent of the same design A later randomised study

(SIRIUS) of more complex stenoses (which are more prone to

recur) still produced a low rate of restenosis within stented

segments (9% v 36% with uncoated stents), even in patients with

diabetes (18% v 51% respectively) Other randomised studies

such as ASPECT and TAXUS II have also shown that coated

stents (with the cytotoxic agent paclitaxel) have significantly

lower six month restenosis rates than identical uncoated stents

(14% v 39% and 6% v 20% respectively) By reducing the

incidence of restenosis (and therefore recurrent symptoms),

drug eluting stents will probably alter the balance of treating

coronary artery disease in favour of percutaneous intervention

rather than coronary artery bypass surgery However, coated

stents will not make any difference to the potential for

percutaneous coronary intervention to achieve acute success in

any given lesion; nor do they seem to have any impact on acute

and subacute safety

Although coated stents may, paradoxically, be too effective at

altering the cellular response and thus delay the desirable

process of re-endothelialisation, there is no evidence that this is

a clinical problem However, this problem has been observed

with brachytherapy (catheter delivered radiotherapy over a

short distance to kill dividing cells), a procedure that is generally

reserved for cases of in-stent restenosis This may lead to late

thrombosis as platelets readily adhere to the “raw” surface that

results from an impaired healing response This risk is

minimised by prolonged treatment with antiplatelet drugs and

avoiding implanting any fresh stents at the time of

brachytherapy

Other energy sources may also prove useful Sonotherapy

(ultrasound) may have potential, less as a treatment in its own

right than as a facilitator for gene delivery, and is “benign” in its

effect on healthy tissue Photodynamic therapy (the interaction

of photosensitising drug, light, and tissue oxygen) is also being

investigated but is still in early development Laser energy, when

delivered via a fine intracoronary wire, is used in a few centres

to recanalise blocked arteries

New work practices

Twenty years ago, a typical angioplasty treated one proximally

located lesion in a single vessel in a patient with good left

ventricular function Now, it commonly treats two or three vessel

disease, perhaps with multiple lesions (some of which may be

complex), in patients with impaired left ventricular function,

advanced age, and comorbidity Patients may have undergone

Names of trials

x ASPECT—Asian paclitaxel-eluting stent clinical trial

x RAVEL—Randomized study with the sirolimus eluting velocity balloon expandable stent in the treatment of patients with de novo native coronary artery lesions

x SIRIUS—Sirolimus-coated velocity stent in treatment of patients with de novo coronary artery lesions trial

x TAXUS II—Study of the safety and superior performance of the TAXUS drug-eluting stent versus the uncoated stent on de novo lesions

Angiograms showing severe, diffuse, in-stent restenosis in the left anterior descending artery and its diagonal branch (L and D, left) This was treated with balloon dilatation and brachytherapy with  irradiation (Novoste) from

a catheter (Br, centre), with an excellent final result (right)

Angiogram of an aortocoronary vein graft with an aneurysm and stenoses (A and S, top) Treatment by implantation of a membrane-covered stent excluded the aneurysm and restored a tubular lumen (bottom)

Bifurcation lesions, such as of the left anterior descending artery and its diagonal branch (L and D, left), are technically challenging to treat but can be well dilated by balloon dilatation and selective stenting (S, right)

Unprotected left main stem stenoses (LMS, top) may, with careful selection,

be treated by stent implantation (S, bottom).

Best results (similar to coronary artery bypass surgery) are achieved in stable patients with good left ventricular function and no other disease.

Close follow up to detect restenosis is important.

descending artery, Cx=

circumflex coronary artery)

ABC of Interventional Cardiology

Trang 5

coronary artery bypass surgery and be unsuitable for further

heart surgery Isolated left main stem and ostial right coronary

artery lesions, though requiring more experience and

variations on traditional techniques, are also no longer a

surgical preserve

Role of percutaneous coronary intervention

The role of percutaneous intervention has extended to the

point where up to 70% of patients treated have acute coronary

syndromes Trial data now support the use of a combination of

a glycoprotein IIb/IIIa inhibitor and early percutaneous

intervention to give high risk patients the best long term results

The same applies to acute myocardial infarction, where

percutaneous procedures achieve a much higher rate of arterial

patency than thrombolytic treatment Even cardiogenic shock,

the most lethal of conditions, may be treated by an aggressive

combination of intra-aortic balloon pumping and percutaneous

intervention

The potential for percutaneous procedures to treat a wide

range of lesions successfully with low rates of restenosis raises

the question of the relative roles of percutaneous intervention

and bypass surgery in everyday practice It takes time to

accumulate sufficient trial data to make long term

generalisations possible

Early trials comparing balloon angioplasty with bypass

surgery rarely included stents and few patients with three vessel

disease (as such disease carried higher risk and percutaneous

intervention was not as widely practised as now) The long term

results favoured bypass surgery, but theses trials are now

outdated In the second generation of studies, stents were used

in percutaneous intervention, improving the results As in the

early studies, surgery and intervention had similarly low

complications and mortality The intervention patients still had

more need for repeat procedures because of restenosis than the

bypass surgery patients, but the differences were less

The major drawback of all these studies was an exclusion

rate approaching 95%, making the general clinical application

of the findings questionable This was because it was unusual at

that time to find patients with multivessel disease who were

technically suitable for both methods and thus eligible for

inclusion in the trials Now that drug eluting stents are available,

more trials are under way: the balance will now probably tip in

favour of percutaneous coronary intervention Meanwhile, the

decision of which treatment is better for a patient at a given

time is based on several factors, including the feasibility of

percutaneous intervention (which is generally considered as the

first option), completeness of revascularisation, comorbidity,

age, and the patient’s own preferences

Implications for health services

These issues are likely to pose major problems for health

services Modern percutaneous techniques can be used both to

shorten patients’ stay in hospital and to make their treatment

minimally hazardous and more comfortable They can also be

used in the first and the last (after coronary artery bypass

surgery) stages of a patient’s “ischaemic career.”

On the other hand, for the role of percutaneous coronary

intervention in acute infarction to be realised, universal

emergency access to this service will be needed However, most

health systems cannot afford this—the main limiting factor

being the number of interventionists and supporting staff

required to allow a 24 hour rota compatible with legal working

hours and the survival of routine elective work

An acute coronary syndrome was found to be due to stenoses and an ulcerated plaque in the right coronary artery (S and U, left) This was treated with a glycoprotein IIb/IIIa inhibitor followed by stent implantation (right) This is an increasingly common presentation of coronary artery disease to catheterisation laboratories

Right coronary artery containing large, lobulated thrombus (T, left) on a substantial stenosis After treatment with glycoprotein IIb/IIIa inhibitor, the lesion was stented successfully (St, right)

General roles of percutaneous coronary intervention (PCI) and coronary artery bypass surgery (CABG)

Condition

PCI

CABG

Acute presentation

Acute coronary syndrome ++ +++ ++ Cardiogenic shock +/ − + +/ − Acute full thickness myocardial infarction + +++ − Bailout after failed thrombolysis + ++ −

Chronic presentation

Impaired left ventricle with left main stem stenosis and blocked right coronary artery

− − − +++ Impaired left ventricle and 3 vessel disease + ++ +++ Impaired left ventricle and 3 vessel disease

with >1 occlusion − + +++ Diabetes and 3 vessel disease + ++ +++ Good left ventricle and 3 vessel disease + ++ +++

2 occluded vessels − − ++ Good left ventricle and 2 vessel disease + +++ ++ Repeat revascularisation after PCI ++ +++ ++ Good left ventricle and 1 vessel disease +++ +++ + 2-3 vessel diffuse or distal disease + ++ + Repeat revascularisation after CABG + ++ + Palliative partial revascularisation + ++ − Revascularisation of frail patient or with

severe comorbidity

+ ++ −

+++ highly effective role, ++ useful role, + limited role, − treatment not preferred, − − treatment usually strongly advised against

Trang 6

The future for percutaneous coronary

intervention

Will percutaneous coronary intervention exist in 20 years time,

or, at least, be recognisable as a logical development of today’s

procedures? Will balloons and stents still be in use? It is likely

that percutaneous procedures will expand further, although

some form of biodegradable stent is a possibility A more

“biological” stent might also be able to act as an effective drug

or gene reservoir, which may extend local drug delivery into

new areas of coronary artery disease We may find ourselves

detecting inflamed (“hot”) plaques with thermography catheters

and treating these before they rupture We may even be able to

modify the natural course of coronary artery disease by

releasing agents “remotely” (possibly using an external

ultrasound trigger) or by injecting an agent that activates the

molecular cargo in a stent

A persistent challenge still limiting the use of percutaneous

coronary intervention is that of chronic total occlusions, which

can be too tough to allow passage of an angioplasty guidewire

An intriguing technique is percutaneous in situ coronary artery

bypass With skill and ingenuity, a few enthusiasts have

anastomosed the stump of a blocked coronary artery to the

adjacent cardiac vein under intracoronary ultrasound guidance,

thereby using the vein as an endogenous conduit (with reversed

flow) This technique may assist only a minority of patients

More practical, we believe, is the concept of drilling through

occlusions with some form of external guidance, perhaps

magnetic fields

“Direct” myocardial revascularisation (punching an array of

holes into ischaemic myocardium) has had a mixed press over

the past decade Some attribute its effect to new vessel

formation, others cite a placebo effect Although the channels

do not stay open, they seem to stimulate new microvessels to

grow Injection of growth factors (vascular endothelial growth

factor and fibroblast growth factor) to induce new blood vessel

growth also has this effect, and percutaneous injection of these

agents into scarred or ischaemic myocardium is achievable

However, we need a more thorough understanding of

biological control mechanisms before we can be confident of

the benefits of this technology

Challenges to mechanical revascularisation

Deaths from coronary artery disease are being steadily reduced

in the Western world However, with increasing longevity, it is

unlikely that we will see a reduction in the prevalence of its

chronic symptoms More effective primary and secondary

prevention; antismoking and healthy lifestyle campaigns; and

the widespread use of antiplatelet drugs, blockers, statins, and

renin-angiotensin system inhibitors may help prevent, or at

least delay, the presentation of symptomatic coronary artery

disease In patients undergoing revascularisation, they are

essential components of the treatment “package.” More effective

anti-atherogenic treatments will no doubt emerge in the near

future to complement and challenge the dramatic progress

being made in percutaneous coronary intervention

Further reading

x Morice M-C, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin

M, et al A randomized comparison of a sirolimus-eluting stent with

a standard stent for coronary revascularization N Engl J Med

2002;346:1773-80

x Park SJ, Shim WH, Ho DS, Raizner AE, Park SW, Hong MK, et al.

A paclitaxel-eluting stent for the prevention of coronary restenosis.

N Engl J Med 2003;348:1537-45

x Raco DL, Yusuf S Overview of randomised trials of percutaneous coronary intervention: comparison with medical and surgical therapy for chronic coronary artery disease In: Grech ED,

Ramsdale DR, eds Practical interventional cardiology 2nd ed.

London: Martin Dunitz, 2002:263-77

x Teirstein PS, Kuntz RE New frontiers in interventional cardiology:

intravascular radiation to prevent restenosis Circulation 2001;104:

2620-6

x Tsuji T, Tamai H, Igaki K, Kyo E, Kosuga K, Hata T, et al.

Biodegradable stents as a platform to drug loading Int J Cardiovasc

Intervent 2003;5:13-6

x Hariawala MD, Sellke FW Angiogenesis and the heart: therapeutic

implications J R Soc Med 1997;90:307-11

x Serruys PW, Unger F, Sousa JE, Jatene A, Bonnier HJ, Schonberger

JP, et al, for the Arterial Revascularization Therapies Study Group Comparison of coronary-artery bypass surgery and stenting for the

treatment of multivessel disease N Engl J Med 2001;344:1117-24

x SoS Investigators Coronary artery bypass surgery versus percutaneous coronary intervention with stent implantation in patients with multivessel coronary artery disease (the stent or

surgery trial): a randomised controlled trial Lancet 2002;360:

965-70

The coronary artery imaging was provided by John Bowles, clinical specialist radiographer, and Nancy Alford, clinical photographer, Sheffield Teaching Hospitals NHS Trust, Sheffield.

Competing interests: None declared.

ABC of Interventional Cardiology

Trang 7

Gerry C Kaye

Before the 1980s, cardiac electrophysiology was primarily used

to confirm mechanisms of arrhythmia, with management

mainly by pharmacological means However, recognised

shortcomings in antiarrhythmic drugs spurred the development

of non-pharmacological treatments, particularly radiofrequency

ablation and implantable defibrillators

The two major mechanisms by which arrhythmias occur are

automaticity and re-entrant excitation Most arrhythmias are of

the re-entrant type and require two or more pathways that are

anatomically or functionally distinct but in electrical contact

The conduction in one pathway must also be slowed to a

sufficient degree to allow recovery of the other so that an

electrical impulse may then re-enter the area of slowed

conduction

Intracardiac electrophysiological

studies

Intracardiac electrophysiological studies give valuable

information about normal and abnormal electrophysiology of

intracardiac structures They are used to confirm the

mechanism of an arrhythmia, to delineate its anatomical

substrate, and to ablate it The electrical stability of the ventricles

can also be assessed, as can the effects of an antiarrhythmic

regimen

Atrioventricular conduction

Electrodes positioned at various sites in the heart can give only

limited data about intracardiac conduction during sinus rhythm

at rest “Stressing” the system allows more information to be

generated, particularly concerning atrioventricular nodal

conduction and the presence of accessory pathways

By convention, the atria are paced at 100 beats/min for

eight beats The ninth beat is premature (extrastimulus), and the

AH interval (the time between the atrial signal (A) and the His

signal (H), which represents atrioventricular node conduction

Tachyarrhythmias

Ischaemic Non-ischaemic

Junctional re-entry tachycardia Atrioventricular

re-entry tachycardia Atrial

ectopy Atrial

fibrillation Atrial

flutter Supraventricular tachycardias Ventricular tachycardias

Concealed accessory pathways

Overt accessory pathways (such as Wolff-Parkinson-White syndrome)

Classification of arrhythmias

Indications for electrophysiological studies Investigation of symptoms

x History of persistent palpitations

x Recurrent syncope

x Presyncope with impaired left ventricular function

Interventions

x Radiofrequency ablation—Accessory pathways, junctional tachycardias, atrial flutter, atrial fibrillation

x Investigation of arrhythmias (narrow and broad complex) with or without radiofrequency ablation

x Assessment or ablation of ventricular arrhythmias

Contraindications

x Severe aortic stenosis, unstable coronary disease, left main stem stenosis, substantial electrolyte disturbance

CSE

CSE

Tricuspid valve

Tricuspid valve

Coronary sinus ostium

Mitral valve

Diagrams showing position of pacing or recording electrodes in the heart in the right anterior oblique and left anterior oblique views (views from the right and left sides of the chest respectively) HRA=high right atrial electrode, usually on the lateral wall or appendage; HBE=His bundle electrode, on the medial aspect of the tricuspid valve; RVA=right ventricular apex; CSE=coronary sinus electrode, which records electrical deflections from the left side of the heart between the atrium and ventricle

A B A

B

Normal

sinus

rhythm

Initiation by premature extrasystole (or extrastimulus) causing unidirectional block due

to longer refractory period down one arm

Tachycardia due

to re-entry continues

Area of slow

conduction

A B

Mechanism of a re-entry circuit An excitation wave is propagated at a

normal rate down path A, but slowly down path B An excitation wave from

an extrasystole now encounters the slow pathway (B), which is still

refractory, creating unidirectional block There is now retrograde

conduction from path A, which coincides with the end of the refractory

period in path B This gives rise to a persistent circus movement

Trang 8

time) is measured This sequence is repeated with the ninth beat

made increasingly premature In normal atrioventricular nodal

conduction, the AH interval gradually increases as the

extrastimulus becomes more premature and is graphically

represented as the atrioventricular nodal curve The gradual

prolongation of the AH interval (decremental conduction) is a

feature that rarely occurs in accessory pathway conduction

Retrograde ventriculoatrial conduction

Retrograde conduction through the atrioventricular node is

assessed by pacing the ventricle and observing conduction back

into the atria The coronary sinus electrode is critically

important for this It lies between the left ventricle and atrium

and provides information about signals passing over the left

side of the heart The sequence of signals that pass from the

ventricle to the atria is called the retrograde activation

sequence

If an accessory pathway is present, this sequence changes:

with left sided pathways, there is an apparent “short circuit” in

the coronary sinus with a shorter ventriculoatrial conduction

time This is termed a concealed pathway, as its effect cannot be

seen on a surface electrocardiogram It conducts retrogradely

only, unlike in Wolff-Parkinson-White syndrome, where the

pathway is bidirectional Often intracardiac electrophysiological

studies are the only way to diagnose concealed accessory

pathways, which form the basis for many tachycardias with

narrow QRS complexes

Supraventricular tachycardia

Supraventricular tachycardias have narrow QRS complexes

with rates between 150-250 beats/min The two common

mechanisms involve re-entry due to either an accessory

pathway (overt as in Wolff-Parkinson-White syndrome or

concealed) or junctional re-entry tachycardia

Accessory pathways

These lie between the atria and ventricles in the atrioventricular

ring, and most are left sided Arrhythmias are usually initiated

by an extrasystole or, during intracardiac electrophysiological

studies, by an extrastimulus, either atrial or ventricular The

extrasystole produces delay within the atrioventricular node,

allowing the signal, which has passed to the ventricle, to re-enter

the atria via the accessory pathway This may reach the

atrioventricular node before the next sinus beat arrives but

when the atrioventricular node is no longer refractory, thus

allowing the impulse to pass down the His bundle and back up

to the atrium through the pathway As ventricular

depolarisation is normal, QRS complexes are narrow This

circuit accounts for over 90% of supraventricular tachycardias in

HBE1-2 V5

CS1-2

CS3-4

CS5-6

CS7-8

CS9-10

HRA3-4

HBE1-2 V5

CS1-2

CS3-4

CS5-6

CS7-8

CS9-10

HRA3-4

A

A

A

A

A

A

A

A

A A

A

A

VP

VP VP

V

V V V V V

V

V V

V

V

Coronary sinus electrode signals, with poles CS9-10 placed proximally near the origin of the coronary sinus and poles 1-2 placed distally reflecting changes in the left ventricular-left atrial free wall Top: normal retrograde activation sequence with depolarisation passing from the ventricle back through the atrioventricular node to the right atrium and simultaneously across the coronary sinus to the left atrium Bottom: retrograde activation sequence in the presence of an accessory pathway in the free wall of the left ventricle showing a shorter ventriculoatrial (VA) time than would be expected in the distal coronary sinus electrodes (CS1-2) Such a pathway would not be discernible from a surface electrocardiogram

Mechanisms for orthodromic (left) and antedromic (right) atrioventricular re-entrant tachycardia

A1A2 (msec)

H1

H2

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0

200

300

400

500

600

700

100

A normal atrioventricular nodal

“hockey stick” curve during antegrade conduction of atrial extrastimuli As the atrial extrastimulus (A 1 -A 2 ) becomes more premature, the AH interval (H 1 -H 2 ) shortens until the atrioventricular node becomes functionally refractory

ABC of Interventional Cardiology

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Wolff-Parkinson-White syndrome Rarely, the circuit is reversed,

and the QRS complexes are broad as the ventricles are fully

pre-excited This rhythm is often misdiagnosed as ventricular in

origin

Treatment—Pathway ablation effects a complete cure by

destroying the arrhythmia substrate Steerable ablation

catheters allow most areas within the heart to be reached The

left atrium can be accessed either retrogradely via the aortic

valve, by flexing the catheter tip through the mitral valve, or

transeptally across the atrial septum Radiofrequency energy is

delivered to the atrial insertion of a pathway and usually results

in either a rapid disappearance of pre-excitation on the surface

electrocardiogram or, in the case of concealed pathways,

normalisation of the retrograde activation sequence Accessory

pathway ablation is 95% successful Failure occurs from an

inability to accurately map pathways or difficulty in delivering

enough energy, usually because of positional instability of the

catheter Complications are rare ( < 0.5%) and are related to

vascular access—femoral artery aneurysms or, with left sided

pathways, embolic cerebrovascular accidents

Junctional re-entry tachycardia

This is the commonest cause of paroxysmal supraventricular

tachycardia The atrioventricular nodal curve shows a sudden

unexpected prolongation of the AH interval known as a “jump”

in the interval The tachycardia is initiated at or shortly after the

jump The jump occurs because of the presence of two

pathways—one slowly conducting but with relatively rapid

recovery (the slow pathway), the other rapidly conducting but

with relatively slow recovery (the fast pathway)—called duality of

atrioventricular nodal conduction This disparity between

conduction speed and recovery allows re-entrance to occur On

a surface electrocardiogram the QRS complexes are narrow,

and the P waves are often absent or distort the terminal portion

of the QRS complex These arrhythmias can often be

terminated by critically timed atrial or ventricular extrastimuli

In the common type of junctional re-entry tachycardia (type

A) the circuit comprises antegrade depolarisation of the slow

pathway and retrograde depolarisation of the fast pathway

Rarely ( < 5% of junctional re-entry tachycardias) the circuit is

reversed (type B) The slow and fast pathways are anatomically

separate, with both inputting to an area called the compact

atrioventricular node The arrhythmia can be cured by mapping

and ablating either the slow or fast pathway, and overall success

occurs in 98% of cases Irreversible complete heart block

requiring a permanent pacemaker occurs in 1-2% of cases, with

the risk being higher for fast pathway ablation Therefore, slow

pathway ablation is the more usual approach

Atrial flutter and atrial fibrillation

Atrial flutter is a macro re-entrant circuit within the right

atrium The critical area of slow conduction lies at the base of

the right atrium in the region of the slow atrioventricular nodal

pathway Producing a discrete line of ablation between the

tricuspid annulus and the inferior vena cava gives a line of

electrical block and is associated with a high success rate in

terminating flutter Flutter responds poorly to standard

antiarrhythmic drugs, and ablation carries a sufficiently

impressive success rate to make it a standard treatment

Atrial fibrillation is caused by micro re-entrant wavelets

circulating around the great venous structures, or it may be

related to a focus of atrial ectopy arising within the pulmonary

veins at their junction with the left atrium The first indication

that atrial fibrillation was electrically treatable came from the

Maze operation (1990) Electrical dissociation of the atria from

the great veins was carried out by surgical excision of the veins

V1 1

CS DIST 1

CS PROX 1

ABL CATH 2.5

V5 1

Surface electrocardiogram leads V1 and V5 and signals from the distal coronary sinus electrodes (CS dist), proximal electrodes (CS prox), and the tip of the ablation catheter (ABL CATH) during pathway ablation to treat Wolff-Parkinson-White syndrome The onset of radiofrequency energy (thin arrow) produces loss of pre-excitation after two beats with a narrow complex QRS seen at the fourth beat (broad arrow) Prolongation of the AV signal in the coronary sinus occurs when pre-excitation is lost

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Atrioventricular nodal curves In a patient with slow-fast junctional re-entrant tachycardia (left) there is a “jump” in atrioventricular nodal conduction when conduction changes from the fast to the slow pathway In a patient with accessory pathways conducting antegradely (such as

Wolff-Parkinson-White syndrome) there is no slowing of conduction as seen

in the normal atrioventricular node, and the curve reflects conduction exclusively over the pathway (right)

Slow pathway

Fast pathway

Slow pathway

Fast pathway Circus

motion

Atrial beat premature

Mechanism of slow-fast junctional re-entrant tachycardia A premature atrial impulse finds the fast pathway refractory, allowing retrograde conduction back up to the atria

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from their insertion sites and then suturing them back The

scarred areas acted as insulation, preventing atrial wave-fronts

from circulating within the atria Similar lines of block can be

achieved by catheter ablation within the right and left atria The

results look promising, although this is a difficult, prolonged

procedure with a high relapse rate Of more interest is a

sub-group of patients with runs of atrial ectopy, which

degenerate to paroxysms of atrial fibrillation These

extrasystoles usually originate from the pulmonary veins, and

their ablation substantially reduces the frequency of

symptomatic atrial fibrillation With better understanding of the

underlying mechanisms and improved techniques, atrial

fibrillation may soon become a completely ablatable

arrhythmia

Ventricular tachycardia

Ventricular tachycardia carries a serious adverse prognosis,

particularly in the presence of coronary artery disease and

impaired ventricular function Treatment options include drugs,

occasional surgical intervention (bypass or arrhythmia surgery),

and implantable defibrillators, either alone or in combination

Ventricular tachycardia can be broadly divided into two groups,

ischaemic and non-ischaemic The latter includes arrhythmias

arising from the right ventricular outflow tract and those

associated with cardiomyopathies

Since the radiofrequency energy of an ablation catheter is

destructive only at the site of the catheter tip, this approach

lends itself more to arrhythmias where a discrete abnormality

can be described, such as non-ischaemic ventricular tachycardia

In ischaemic ventricular tachycardia, where the abnormal

substrate often occurs over a wide area, the success rate is lower

Ideally, the arrhythmia should be haemodynamically stable,

reliably initiated with ventricular pacing, and mapped to a

localised area within the ventricle In many cases, however, this

is not possible The arrhythmia may be unstable after initiation

and therefore cannot be mapped accurately The circuit may

also lie deep within the ventricular wall and cannot be fully

ablated However, detailed intracardiac maps can be made with

multipolar catheters A newer approach is the use of a

non{contact mapping catheter, which floats freely within the

ventricles but senses myocardial electrical circuits

Although the overall, long term, success rate for

radiofrequency ablation of ischaemic ventricular tachycardia is

only about 65%, this may increase

Conclusion

The electrophysiological approach to treating arrhythmias has

been revolutionised by radiofrequency ablation Better

computerised mapping, improved catheters, and more efficient

energy delivery has enabled many arrhythmias to be treated

and cured The ability to ablate some forms of atrial fibrillation

and improvement in ablation of ventricular tachycardia is

heralding a new age of electrophysiology Ten years ago it could

have been said that electrophysiologists were a relatively benign

breed of cardiologists who did little harm but little good either

That has emphatically changed, and it can now be attested that

electrophysiologists exact the only true cure in cardiology

Diagram of basket-shaped mapping catheter with several recording electrodes (red dots) The basket retracts into a catheter for placement in either the atria or ventricles.

Once it is in position, retraction of the catheter allows the basket to expand

Further reading

x Olgin JE, Zipes DP Specific arrhythmias: diagnosis and treatment.

In: Braunwald E, Zipes DP, Libby P, eds Heart disease 6th ed.

Philadelphia: Saunders, 2001:1877-85

x McGuire MA, Janse MJ New insights on the anatomical location of components of the reentrant circuit and ablation therapy for

atrioventricular reentrant tachycardia Curr Opin Cardiol 1995;

10:3-8

x Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, et al Treatment of supraventricular tachycardia due to atrioventricular nodal re-entry by radiofrequency catheter ablation

of the slow-pathway conduction N Engl J Med 1992;327:313-8

x Calkins H, Leon AR, Deam AG, Kalbfleisch SJ, Langberg JJ, Morady F Catheter ablation of atrial flutter using radiofrequency

energy Am J Cardiol 1994;73:353-6

x Schilling RJ, Peter NS, Davies DW Feasibility of a non-contact catheter for endocardial mapping of human ventricular

tachycardia Circulation 1999;99:2543-52

Competing interests: None declared.

The diagrams showing the mechanisms of orthodromic and antedromic atrioventricular re-entrant tachycardia and of slow-fast atrioventricular nodal re{entrant tachycardia are reproduced from ABC of Clinical

Electrocardiography, edited by Francis Morris, 2002.

ABC of Interventional Cardiology

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